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Introduction
Gastroenteritis is defined as the inflammation of the mucus membranes of the gastrointestinal
tract and is characterized by diarrhea or vomiting. It is a common childhood disease. Children in
developing countries are particular at risk of both morbidity and mortality. Worldwide,
gastroenteritis affects 3 to 5 billion children each year, and accounts for 1.5 to 2.5 million deaths
per year or 12% of all deaths among children less than 5 years of age.1–3 In developed countries,
such as the United States, acute gastroenteritis seldom causes deaths, however, it still accounts
for 300 deaths per year.2 Moreover, it puts a heavy burden on the health care system. Acute
gastroenteritis causes 1.5 million visits to primary care providers each year and 220,000 hospital
admissions for children under the age of 5 years; that is 10% of all the hospital admissions of
children in the United States.2 In general, developing countries have a higher rate of hospital
admissions as compared to developed countries. In the United States, the admission rate is 9 per
1000, per annum, for children younger than 5 years old.4 When compared to the United
Kingdom and Australia, the admission rates are around 12 to 15 per 1000 per
annum.5,6 However, the rate increases dramatically to 26 per 1000 per annum in China.7 This
may be due to the facts that children in developed countries have a better nutrition status and
better primary care. The difference can also be explained by the fact that, the incidence of acute
gastroenteritis is significantly higher in developing countries than the industrialized
countries.8 Interestingly, Hong Kong is a developed city, and yet the admission rate is even
higher than many of the developing countries.9 This may reflect that the decision of admission
does not simply depend on the clinical situations, but it can also be affected by the parents’
wishes and other social factors.
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Etiology
Viruses are the most important etiology and are responsible for approximately 70% of the
episodes of acute gastroenteritis in children.10 There are over 20 different types of viruses that
have been identified as etiological agents.11 Worldwide, rotavirus is still the most common virus
causing this disease and accounts for some 30% to 72% of all the hospitalizations and 4% to
24% of acute gastroenteritis at the community level.12–15 Virtually all children have been
infected with rotavirus by the age of 3 years.16 Rotavirus infection is seasonal in temperate
climates, peaking in late winter, although it occurs throughout the year in the tropics. The peak
age for infection ranges from 6 months to 2 years. Other common viruses causing gastroenteritis
include calicivirus, adenovirus and astrovirus. Globally these viruses are responsible for diarrhea
episodes in hospitalized children, with detection rates varying from 3.2%–29.3%, 1%–31%, and
1.8%–16%, respectively.17–20 Rates of virus infection are similar in both developed and less
developed countries.21 Bacterial infection accounts for 10% to 20% of all the acute
gastroenteritis.22 The most common bacterial causes
are, Salmonella species, Campylobacter species, Shigella species and Yersina species. Vibrio
cholerae remains a major cause of diarrhea, especially after a disaster where sanitation is
compromised. Giardia lamblia is the most common protozoal infection that causes
gastroenteritis, although it tends to be associated with more persistent diarrhea. Other protozoa
include Cryptosporidium species and Entamoeba histolytica. However, less developed countries
have a higher rate of parasites and Escherichia coli infection which are both relatively
uncommon in the industrialized countries.21 This indicates that improvement in sanitation will
not decrease the disease prevalence of viral infection but can help in prevention of parasites and
bacterial infections.
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Rotavirus as a prototypic virus for gastroenteritis

Rotavirus is a prototypical virus because it is the most common virus that causes acute
gastroenteritis in children which results in hospitalization and treatment with intravenous fluid.
According to the data from the United States, approximately 410,000 physician visits are due to
the rotavirus infection, the cause of 205,000 to 272,000 emergency department visits, which
results in 55,000 to 70,000 hospitalizations.23 In the United States, 1 in 67–85 children will be
hospitalized because of rotavirus infection by the age of 5 years.24 On the other hand, Hong
Kong has a very high rate of hospitalization. By the age of 5 years, the cumulative risk is 1 in 24,
a figure that is 3 times higher than the that of the United States.9 For each admission in the
United States, the hospital costs range from $2999 to $3400 with the family costs being $359
which includes the caregivers loss of work.24–26 In Hong Kong, admission costs are less
expensive although they are not unsubstantial at $1868 (US) for each admission and $120 for
family expenses.9 Adding in the prevalence of the disease, gastroenteritis causes a significant
economic burden to the health care system. As to the severity of the disease, a study that
included 234 hospitalized children infected with rotavirus, 63% of them had diarrhea, vomiting
and fever, 21% had diarrhea and vomiting, 7% had diarrhea and fever, 4% had vomiting and
fever, 3% had fever alone, 2% had vomiting alone and 0.4% had diarrhea alone.27 In general,
90% of the hospitalized patients had vomiting. Vomiting is one of the most important symptoms
for considering failure of oral rehydration therapy and requiring intravenous therapy.28,29
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Oral rehydration therapy versus intravenous therapy

The American Academy of Pediatrics (AAP), Centers for Disease Control and Prevention
(CDC), European Society for Pediatric Gastroenterology and Nutrition, and the World Health
Organization (WHO) all strongly support the use of oral rehydration therapy as the first-line
therapy for the treatment of acute gastroenteritis, except in cases of severe dehydration.2,30–
32 The effectiveness of oral rehydration therapy in treating acute gastroenteritis, with mild to
moderated dehydration, has been demonstrated by many randomized controlled trials. In a
Cochrane meta-analysis of 17 trials from 1982 to 2005, in which 9 trials were from the
developed countries, 7 trials from developing countries and 1 trial involving developed and less
developed countries.33 Included in this analysis were more than 1800 participants. The data
showed that there were no important clinical differences between oral hydration therapy and
intravenous therapy for rehydration secondary to acute gastroenteritis in children; and that
children treated with oral rehydration therapy spent less time in hospitals. Moreover, patients
receiving intravenous therapy had a 2.5% risk of phlebitis that did not occur in the oral
rehydration group. Importantly, this result is unlikely to change with further trials because there
is already adequate power to support the observed results and further research comparing oral
rehydration therapy and intravenous therapy is not warranted and may be unethical. The
effectiveness of oral rehydration therapy is not isolated to just clinical trials it can also be
reflected in the decreased mortality rate. In 1970’s the diarrheal illness related deaths were 4.6
million/year worldwide.34 After the promotion of oral rehydration therapy by World Health
Organization (WHO) at the end of 1970’s, the diarrheal illness related death rate dropped to 3.3
million/year in 1980’s, with a further drop to 2.5 million/year in 1990’s.35
The oral rehydration solution is regarded as one of the most important medical advances of the
20th century. Although there is much evidence to support the usage of oral rehydration with
numerous published guidelines and many professional organizations recommending its use, oral
rehydration solution is still described as an underused simple therapy.36 Intravenous therapy is
still often chosen rather than oral rehydration therapy. Data from Europe, Australia and Canada
show that 80% to 94% of hospitalized children do not have any signs of dehydration and yet they
still receive intravenous therapy.37–39 Data from Hong Kong, that assessed more than 7000
episodes of admission due to gastroenteritis in children under 5 years of age, also showed that
only 1.3% to 8.4% had signs of dehydration and yet up to 48% of the patients received
intravenous therapy.40 The rate of intravenous therapy was even higher in the rotavirus group.
According to a recent survey, 45% of physicians still preferred intravenous fluid therapy rather
than oral rehydration therapy in treating moderate dehydration in acute
gastroenteritis.41 However, judging the effectiveness of oral rehydration therapy and the overuse
of the intravenous therapy, any treatments in acute gastroenteritis should improve the success or
compliance of oral rehydration therapy as the top priority. Safety and cost are also important
issues. Successful oral rehydration therapy always means that the children can be managed in the
community. It is more pleasant for the children and more comfortable for the caregivers. Oral
rehydration therapy also helps to save money by reducing the hospitalization costs.
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Reasons of underused oral rehydration therapy

The reasons for the underuse of oral rehydration therapy are not fully understood. In 2002 Ozuah
and colleagues published a national random survey of emergency physicians selected from the
mailing list of the AAP that addressed this issue.29 A total of 176 physicians responded (73%
response rate). Their responses can be divided into four categories: the physician factors; patient
factors; parental concern; and environment or social factors. Regarding the physician factors; in
contrast to the group of physicians unfamiliar with the AAP guidelines, the familiar group was
more likely to use oral rehydration therapy in scenarios of mild dehydration (81% versus 66%)
and moderate dehydration (25% versus 10%). Parental concern about dehydration (disregarding
the actual hydration status of the patients) would make 31% of the emergency department
physicians choose intravenous therapy over oral rehydration therapy. A crowded or emergency
department with long waiting times would cause 22% of the physicians to choose intravenous
therapy. Regarding the severity of dehydration, 49.4% of emergency department physicians
would offer intravenous therapy even in moderate dehydration. In terms of symptoms, only 8%
of the emergency department physicians would consider intravenous therapy when diarrhea was
a major symptom. On the other hand, patients refusing to drink was the most likely reason for
choosing intravenous therapy (up to 96%). Vomiting was the second most important reason
given for intravenous therapy, with up to 85% of the physicians being more likely to use
intravenous therapy when vomiting was the predominant symptom. In another study, up to 36%
of the surveyed physicians believed that vomiting was a contraindication for oral rehydration
therapy.28
Approximately 70% of all children with gastroenteritis also present with vomiting.37 According
to our own unpublished data (of more than 7000 episodes of hospitalization in Hong Kong due to
acute gastroenteritis in children younger than 5 years of age) 62% of gastroenteritis patients
presented with vomiting. Up to 82% of rotavirus infected children presented with vomiting, a
figure that was very similar to the study by Staat and colleagues in 2002.27 In terms of the
episodes and duration of vomiting in gastroenteritis patients, the mean number of vomiting
episodes was 4.91/24 hours and for a duration of 1.84 days. In summary this may partly explain
why the oral rehydration solution is an underused simple solution.
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The pathophysiology of vomiting and the mechanisms of antiemetic

medications
Vomiting is usually defined as a violent expulsion of the stomach contents through the mouth
and being a very unpleasant symptom. It can also be associated with nausea and retching. The
mechanism of vomiting has been well characterized, first by Borison and Wang in 1953.42 The
vomiting center controls and integrates the act of vomiting. It is located in the lateral reticular
formation of the medulla oblongata, which is close to other centers that regulate respiration,
vasomotor, and other autonomic functions. These centers too may also play an additional role in
vomiting. Emetic stimuli can be transmitted directly to the vomiting center or through the
chemoreceptor trigger zone. The chemoreceptor trigger zone, located in the area postrema of the
fourth ventricle and outside the blood-brain barrier, is exposed to both cerebrospinal fluid and
blood.43 This would allow the chemoreceptor trigger zone to pick up the chemical signals from
both cerebrospinal fluid and blood stream (such as bacterial toxins or form metabolic
abnormalities that occur with uremia) and act as an afferent limb to the vomiting center;
however, it cannot independently mediate the act of vomiting without the interaction of vomiting
center. On the other hand, the vomiting center does not only receive information from the
chemoreceptor trigger zone, it can also receive information and stimulation from the cerebral
cortex and limbic system, the vestibular system, and the vagal and splanchnic
afferents.42,44,45 Psychological stress such as fear can act on cerebral cortex and limbic system
to induce vomiting via the vomiting center. Vomiting due to motion sickness develops
consequent to stimulation of the vestibular system, with impulses that travel from the labyrinth
of the inner ear to the vomiting center.
However, the exact mechanism of vomiting in gastroenteritis is not known; although it is thought
to be due to the peripheral stimuli arising from the gastrointestinal tract primarily via the vagus
nerve or via serotonin stimulation of the 5-hydroxytryptamine 3 (5HT3) receptors in the gut.46–
49 In acute gastroenteritis, intestinal irritation can damage the gastrointestinal mucosa and result
in the release of serotonin from the enterochromaffin cells. This serotonin acts on the 5HT3
receptors of the vagal afferent nerves in the gastrointestinal tract,49 which are then transmitted to
the vomiting center directly or via the chemoreceptor trigger zone. The vomiting center then
sends efferent impulses to the diaphragm, abdominal muscles, and visceral nerves of the stomach
and esophagus to produce vomiting.50,51 These events typically include: an increase in
salivation; a decrease in gastric tone that results in the sensation of nausea; nonperistaltic
contractions in the small intestine; regurgitation of the intestinal contents into the stomach;
contractions of the respiratory and abdominal muscles; and the descent of the diaphragm against
a closed glottis such that the gastric contents are forced up into the esophagus and out through
the mouth.
Antiemetic therapy aims at: depressing the vomiting center; depressing the chemoreceptor
center; inhibiting the impulses from chemoreceptor zone to vomiting center; and/or inhibiting
impulses from peripheral receptors to the vomiting center. All the areas involved in the
pathogenesis of vomiting are rich in serotoninergic, dopaminergic, histaminic, and muscarinic
receptors.45 Dopamine antagonists suppress proemetic stimuli by blocking D2 receptors in the
chemoreceptor trigger zone. 5-HT3 antagonists have been more recently developed to block the
nausea and vomiting reflexes mediated by stimulation of 5-HT3 receptors in both the small
intestine and the chemoreceptor center. Antihistamines, although widely used for migraine, are
generally recommended for motion sickness as they act at the level of the vestibular
apparatus.43,52 Anti-cholinergic agents such as atropine and hyoscine are relatively ineffective
in the treatment or prevention of vomiting due to causes other than motion sickness.52–54 The
mechanism of action is not clearly understood in some antiemetic medications such as
dexamethasone and trimethobenzamide.
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The use of antiemetics in acute gastroenteritis

In 1996, the AAP made the following statement: “The committee did not evaluate the use of
antiemetic drugs. Consensus opinion is that antiemetic drugs are not needed. Physicians who feel
that antiemetic therapy is indicated in a given situation should be aware of potential adverse
effects”.31 In 2003, the Centers for Disease Control and Prevention (CDC) released an updated
statement regarding the usage of antiemetics. It also concluded that antiemetics are usually
unnecessary. Reliance on pharmacologic agents shifts the therapeutic focus away from
appropriate fluid, electrolyte, and nutritional therapy, that can result in adverse events, and can
add unnecessarily to the economic burden of the illness.2 Notwithstanding the lack of an official
recommendation for their use, antiemetics are still commonly prescribed among different
specialties and countries in the management of acute gastroenteritis.
Antiemetics are often used because vomiting is an unpleasant and a distressing symptom which
can increase the likelihood of dehydration, electrolyte imbalance, pulmonary aspiration, and
most importantly the need for intravenous hydration or hospitalization.55–58 The reasons why
antiemetics are not commonly recommended for gastroenteritis related vomiting are because
vomiting is self-limiting, vomiting is a normal physiological reaction for ridding the body of
toxic substances, and antiemetics can have adverse side effects.10,38,59 In addition, the newer
antiemetics are also costly.
O’Loughlin and colleagues prospectively surveyed all children with acute vomiting or diarrhea
who were admitted to a pediatric inpatient facility in Newcastle, NSW, Australia, during a 12-
month period. The authors found that antiemetic medication was administered to 21 (9%) of 231
children prior to admission.59 Elliott and colleagues found that antiemetic medications were
prescribed for the treatment of acute gastroenteritis in 9 (5.5%) of 164 children prior to
admission to the Royal Alexandra Hospital for Children in Sydney, NSW, Australia, during a 6-
month period.38 Nelson and colleagues interviewed the caregivers of 105 pediatric in-patients
with gastroenteritis in Hong Kong where up to 73% had seen one or more primary care
practitioners prior to admission to hospital, and 29% of cases were prescribed antiemetics.60
In 2002, Kwon and colleagues conducted a national survey to address this problem in the United
States among emergency physicians, general pediatricians and pediatric emergency
physicians.61 In this study, 79.2% of emergency physicians would prescribe antiemetics as
compared to 52.2% of general pediatricians and 55.2% of pediatric emergency physicians. The
use of antiemetics by emergency physicians was greater than the other two specialties (P <
0.001). The most commonly nonexclusive reason for prescribing antiemetic use was to prevent
the worsening dehydration and the need for subsequent intravenous fluids or admission (72.0%).
This was followed by patient comfort (59.0%), assurance/documentation of oral liquid trial in
emergency department/clinic/office before discharge (35.5%), and parental concerns/pressures
(29.4%). Albano and colleagues conducted a similar survey to look at the practice of Italian
hospital pediatricians and family physicians.62 Approximately 71% of hospital pediatricians
would use antiemetic medications as compared to 96% of the family physicians. When
comparing the reasons for prescription by family physicians versus hospital pediatricians, the
latter were more likely to prescribe antiemetics in order to increase the success rate of oral
rehydration therapy (48%), whereas family physicians prescribed them to increase patient
comfort or to reduce concerns of parents (46%).
Pfeil and colleagues investigated the prescription pattern of antiemetic medications in 0- to 9-
year-old children with infectious gastroenteritis in several industrialized countries during
2005.63 The authors retrospectively retrieved data from four national and international databases
which showed that between 2% and 23% of children with gastroenteritis received prescriptions
for antiemetic medications (United States, 23%; Germany, 17%; France, 17%; Spain, 15%; Italy,
11%; Canada, 3%; United Kingdom, 2%).
In summary, antiemetic drugs are frequently used in children with gastroenteritis by physicians
in various specialties and in various countries in spite of the lack of an official recommendation
for their use.
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Antiemetic medications

Serotonin 5HT3 receptor antagonists

Ondansetron
Ondansetron is a carbazole derivative that has been available since 1991. It is one of the best
known potent serotonin 5-HT3 receptor-antagonists that blocks receptors at the vagus and
sympathetic nerves together with the chemoreceptor trigger zones.64 It has no antidopaminergic
properties. The efficacy of ondansetron for chemotherapy-induced or postoperative vomiting in
the pediatric population is well documented.65,66 It also has promising effects in patients with
vomiting due to migraines, procedural sedation with ketamine and acetaminophen poisoning.67–
69
These positive results initiated investigations for their use in gastroenteritis related vomiting.
However, only a few randomized controlled trials regarding its use in pediatric gastroenteritis
have been published. In 2008, DeCamp and colleagues published a meta-analysis in order to
address this question.70 The investigators reviewed prospective controlled trials only and looked
at the emesis cessation, use of intravenous fluid for rehydration, hospital admission, return to
care, and medication adverse effects as the principal outcomes. There were 11 articles that met
the inclusion criteria. Ondansetron has the greatest number of studies that met the criteria (n = 6,
participants = 745).55,71–75 All of the studies were conducted in the emergency department
setting, except the study by Cubeddu and colleagues that was performed in an in-patient
setting.55 The majority of studies included only children but the study by Reeves and colleagues
also included patients up to 22 years of age.72 Among the six studies, the two studies published
by Reeves et al and Freedman et al required dehydration as an inclusion criterion.72,74 The
study published by Roslund and colleagues and Stork and colleagues, required both dehydration
and failure of oral rehydration as the inclusion criteria.71,75 However, all the participants in the
study by Stork and colleagues received intravenous therapy.71 In all except one study, only one
dose of ondansetron was administered during the study period. The study by Ramsook and
colleagues provided families with additional doses for home use.73 Routes of administration and
dosing varied across studies. There were 3 studies using intravenous ondansetron. Among these
3 studies, both Stork et al and Reeves et al used a dose of 0.15 mg/kg,71,72 whereas Cubeddu
and colleagues used a dose of 0.3 mg/kg.55 Among the 3 studies of oral ondansetron, Freedman
et al and Roslund et al used similar weight-based dosing ranging from 2 to 8 mg,74,75 and
Ramsook and colleagues used age-based dosing ranging from 1.6 to 4.0 mg.73 The follow-up
period ranged from 24 hours to 2 weeks.
Five studies (659 participants) reported whether patients continued to have emesis in the
emergency department after administration of the study drug. Using data from these five studies,
the relative risk (RR) for vomiting after the ondansetron compared to placebo was 0.45 (95%
confidence interval [CI]: 0.33–0.62; number needed to treat [NNT] = 5).70 Four studies (489
participants) reported the use of intravenous fluid. However, the indications for intravenous fluid
varied from study to study and included persistent emesis, refusal to drink, and persistent or
worsening states of dehydration. It also showed a statistically significant reduction in the RR of
intravenous fluid use for patients who received ondansetron versus placebo (RR, 0.41; 95% CI:
0.28–0.62; NNT = 5).70 Five trials (662 participants) included hospital admission as an outcome.
Patients who received ondansetron had a statistically significant decrease in risk of immediate
hospital admission (RR, 0.52; 95% CI: 0.27–0.95; NNT = 14).70 Five trials (612 participants)
assessed whether patients returned to outpatient care during the study period. Ondansetron use
did not significantly affect return to care (RR, 1.34; 95% CI: 0.77–2.35).70 With regard to the
RR of admission during the whole study period, there was also no significant difference between
the treatment group and the controlled group (RR, 0.69; 95% CI: 0.43–1.11).70
Five studies documented the severity of diarrhea after ondansetron administration. Overall, three
studies have documented an increased severity of diarrhea after the ondansetron. Freedman and
colleagues reported an increase in diarrhea during the emergency department stay although they
did not evaluate the incidence of diarrhea during follow-up.74 Ramsook and colleagues did not
detect any difference in the severity of diarrhea during the emergency department stay but
reported an increase in severity in 48 hours after discharge from the emergency
department.73 Cubeddu and colleagues also reported more diarrhea episodes in the 24 hours
after the ondansetron administration.55 On the other hand, the studies by Roslund et al and
Reeves et al detected no differences in diarrheal episodes 5 to 7 days after discharge from the
emergency department.72,75 In summary, although an increase in diarrhea was noted in the
ondansetron group up to 48 hours after administration, no difference in frequency was detected
afterwards. No other adverse event was systemically evaluated and no other adverse effects were
common across different studies.
The most recent Cochrane meta-analysis was performed by Alhashimi and colleagues who used
very strict inclusion criteria and excluded the studies by Reeves et al and Stork et al.76 The
authors came to a similar conclusion, that ondansetron may reduce the amount of acute vomiting
as well as reducing the number of children who required intravenous rehydration, and admission
for acute gastroenteritis. However, participants in the ondansetron group did have more diarrhea
than in the placebo group.
There was one randomized, double blind, placebo controlled trial that was published in 2009,
however, it was not included in the previous meta-analysis.77 This study was also performed in
emergency department. A total of 109 children aged from 5 months to 8 years who had
nonbilious, nonbloody vomiting at least 4 times in the last six hours, who could not tolerate oral
feeding, who had at least 4 episodes of diarrhea in the previous 24 hours, and who had mild to
moderate dehydration were recruited. Oral ondansetron (0.2 mg/kg/dose) was administered at 8
hourly intervals with a total of 3 doses. The frequency of vomiting was significantly lower
among the children who received ondansetron than among those who received placebo (0.36
versus 1.33, P < 0.001 and 0.2 versus 1.66, P < 0.001 at four hours and twenty-four hours
respectively). Weight gain in the ondansetron group was significantly higher than that of the
placebo group at eight hours after intervention. At the end of the study, 5.4% (3/55) in the
ondansetron group and 18.6% (10/54) in the placebo group failed oral rehydration therapy (RR =
0.29; 95% CI: 0.086–1.01; P = 0.04). The authors found that the absolute risk of reduction and
the number needed to treat were 13.2% and 8%, in terms of hospitalization and/or intravenous
rehydration treatment. In terms of side effects, the children who received ondansetron had more
episodes of diarrhea while undergoing oral rehydration than those who received placebo at 24
hours (P = 0.04). All of the randomized controlled trials (RCT) evaluating the efficacy of
ondansetron in acute gastroenteritis are summarized in Table 1.
Table 1
Summary of randomized controlled trials evaluating the efficacy of ondansetron in acute
gastroenteritis
Source Settin N Age Inclusion Antiemetic agent Route/dos Outcomes Side Follo
g o. criteria e of effect w-up
ondansetr s
on

Cubed Inpatie 36 6 GE and Ondansetron/Metoclopr IV Vomiting Increa 24 hrs

du et al nt mont >2 × amide (0.3mg/kg 0.3 mg/kg episodes and se in
199755 h–8 emesis iv)/isotonic saline single ORT failure diarrh
years within 1 dose ea
hours

Ramso ED 14 6 GE with Ondansetron (syrup) PO Vomiting Increa 24 hrs

ok et al 5 mont >5 × 6m–1 episodes, se in
200273 h–12 vomiting year: 1.6 receipt of diarrh
years in the mg IVF, ea
preceding 1–3 year: hospital
24 hours 3.2 mg/4– admission,
12 year: 4 and diarrheal
mg episode
Q8H up to
6 doses

Reeves ED 10 1 GE and Ondansetron IV Vomiting No 5–7

et al 7 mont >3 × 0.15 episodes, increa days
200272 h–22 vomiting mg/kg hospital se in
years in the Single admission, diarrh
preceding dose duration of ea
24 hours, vomiting,
requiring diarrhea
Source Settin N Age Inclusion Antiemetic agent Route/dos Outcomes Side Follo
g o. criteria e of effect w-up
ondansetr s
on

IV episodes,
rehydrati and return to
on ED and need
for
readministra
tion of IVF

Stork ED 13 6 GE, >3 × Onsansetron/Dexameth IV

et al 7 mont emesis asone
200671 h–12 within (1mg/kg)/isotonic
years past 24 saline
hours,
mild to
moderate
dehydrati
on, and
failed
oral
hydration